ROS signaling in the hypersensitive response When, where and what for?

被引：129

作者：

Zurbriggen, Matias D. ^{[1
]}

Carrillo, Nestor ^{[1
]}

Hajirezaei, Mohammad-Reza ^{[2
]}

机构：

[1] Univ Nacl Rosario, CONICET, Inst Biol Mol & Celular Rosario IBR, Rosario, Santa Fe, Argentina

[2] Leibniz Inst Plant Genet & Crop Plant Res Leibniz, Gatersleben, Germany

来源：

PLANT SIGNALING & BEHAVIOR | 2010年 / 5卷 / 04期

关键词：

biotic stress; chloroplasts; flavodoxin; hypersensitive response (HR); reactive oxygen species (ROS); ROS signaling;

D O I：

10.4161/psb.5.4.10793

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Plants generally react to the attack of non-host and incompatible host microorganisms by inducing pathogenesis-related (PR) genes and localised cell death (LCD) at the site of infection, a process collectively known as the hypersensitive response (HR). Reactive oxygen species (ROS) are generated in various sub-cellular compartments shortly after pathogen recognition, and proposed to cue subsequent orchestration of the HR. Although apoplast-associated ROS production by plasma membrane NADPH oxidases have been most thoroughly studied, recent observations suggest that ROS are generated in chloroplasts earlier in the response and play a key role in execution of LCD. A model is presented in which the initial outcome of successful pathogen detection is ROS accumulation in plastids, likely mediated by mitogen-activated protein kinases and caused by dysfunction of the photosynthetic electron transport chain. ROS signaling is proposed to spread from plastids to the apoplast, through the activation of NADPH oxidases, and from there to adjacent cells, leading to suicidal death in the region of attempted infection.

引用

页码：393 / 396

页数：4

共 29 条

[11] Evidence of mitochondrial involvement in the transduction of signals required for the induction of genes associated with pathogen attack and senescence [J].